The Legacy of Joseph A. Moylan, M.D.: “It’s About Everyone Else”

The history of modern American surgery is marked by larger-than-life pioneers who have made transformative contributions to our field. These extraordinary individuals have been known primarily for their technical and clinical mastery, development of novel surgical procedures and techniques, extraordinary abilities in the education and training of surgeons, and/or innovative discoveries in biomedical science. While mastery in clinical surgery, education, and research have come to characterize the consummate academic surgeon, challenging social inequities of today now demand deeper engagement in another vital arena. This historical account is the story of a truly exceptional surgeon and visionary who spent much of his life leading that very charge. Early in his career, Dr. Joseph Moylan recognized and embraced this obligation to go beyond the walls of the hospital and out into the community to combat social factors leading to adverse outcomes for at-risk young men. His legacy itself represents a vehicle for empowering youth confronted with barriers to educational opportunities and experiences. Furthermore, recounting Joe’s journey conveys the over-arching thesis that surgeons have the opportunity—and, indeed, are well positioned—to engage more deeply with their communities, to lead efforts to address social determinants at their roots and to create a pipeline of bright young scholars and potential future surgeons

Cholinergic modulation of microglial activation by alpha 7 nicotinic receptors.

Almost all degenerative diseases of the CNS are associated with chronic inflammation. A central step in this process is the activation of brain mononuclear phagocyte cells, called microglia. While it is recognized that healthy neurons and astrocytes regulate the magnitude of microglia-mediated innate immune responses and limit excessive CNS inflammation, the endogenous signals governing this process are not fully understood. In the peripheral nervous system, recent studies suggest that an endogenous \u27cholinergic anti-inflammatory pathway\u27 regulates systemic inflammatory responses via alpha 7 nicotinic acetylcholinergic receptors (nAChR) found on blood-borne macrophages. These data led us to investigate whether a similar cholinergic pathway exists in the brain that could regulate microglial activation. Here we report for the first time that cultured microglial cells express alpha 7 nAChR subunit as determined by RT-PCR, western blot, immunofluorescent, and immunohistochemistry analyses. Acetylcholine and nicotine pre-treatment inhibit lipopolysaccharide (LPS)-induced TNF-alpha release in murine-derived microglial cells, an effect attenuated by alpha 7 selective nicotinic antagonist, alpha-bungarotoxin. Furthermore, this inhibition appears to be mediated by a reduction in phosphorylation of p44/42 and p38 mitogen-activated protein kinase (MAPK). Though preliminary, our findings suggest the existence of a brain cholinergic pathway that regulates microglial activation through alpha 7 nicotinic receptors. Negative regulation of microglia activation may also represent additional mechanism underlying nicotine\u27s reported neuroprotective properties

ON T2* MAGNETIC RESONANCE AND CARDIAC IRON

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